The postnatal development of mammalian skeletal muscle is characterized by an increased capacity for glycogen metabolism. The hormones, insulin and epinephrine, regulate glycogen synthesis and degradation via the control of cAMP levels in the muscle cell. The receptors and effector enzymes for insulin and epinephrine are located in the muscle cell plasma membrane (sarcolemma). This proposal seeks to determine the development of the insulin and beta-adrenergic receptors in developing skeletal muscle sarcolemma. It is hypothesized that receptor development and/or coupling of receptor activation to effector enzyme stimulation may serve as a developmental signal for the metabolic pathways the hormone-receptor interaction modulates. Studies completed in the second year of the proposal show that the expression of epinephrine-stimulated adenylate cyclase activity involves an increase in adenylate cyclase activity with no alteration in the number of beta-adrenergic receptors. The parallel increase in sarcolemma linoleic acid concentration may reflect a mechanism by whiich increased membrane fluidity promotes beta-receptor coupling to adenylate cyclase during muscle development. Studies are now being inaugurated to determine the 1) mechanisms involved in the control of sarcolemma linoleic acid concetration, and 2) relationship between sarcolemma alterations in the beta-adrenergic response and the control of glycogenolysis during postnatal muscle development.